In earlier studies a variety of substituted hydrazines were found to produce liver injury due to their further metabolic conversion, in vivo, to acylating or aklylating agents. There is precedent to suggest that aminohydantoin (AH) could be formed in vivo as a degradation product from either nitrofurantoin or Dantrium. Since AH can be viewed as a substituted hydrazine, we are investigating it as a possible causative factor in hepatic damage produced in patients by these drugs.